Key result
FoxO6 deficiency attenuated contractile dysfunction and cardiac remodeling in Ang-II-treated mice, whereas FoxO6 overexpression aggravated cardiomyopathy via the Kif15/TGF-β1 axis.
Why the study?
Pathological cardiac hypertrophy exhibits abnormal gene expression and progresses to heart failure, but the role of transcription factor FoxO6 in cardiac hypertrophy remains to be explored.
Does FoxO6 deficiency prevent Ang-II-induced cardiac remodeling and dysfunction in mice?
Population
Wild-type, FoxO6 knockout, and FoxO6-overexpressing mice
Comparison
Daily administration of angiotensin-II vs saline
Design
Preclinical animal and in vitro study
Follow-up
4 weeks
Authors
Loading...
Hypothesis-generating for FoxO6 inhibition in pressure-overload models; leaves open translation to human heart failure therapy.
Does FoxO6 deficiency prevent Ang-II-induced cardiac remodeling and dysfunction in mice?
FoxO6 promotes pathological cardiac remodeling and dysfunction under aggravated afterload by activating the Kif15/TGF-β1 axis, identifying a potential novel therapeutic target for heart failure.
Zhang et al. (2023) studied Cardiac hypertrophy. FoxO6 genetic manipulation (knockout or overexpression) vs. Wild-type mice was evaluated on Cardiac hypertrophy, fibrosis, and function. FoxO6 deficiency attenuated contractile dysfunction and cardiac remodeling in Ang-II-treated mice, whereas FoxO6 overexpression aggravated cardiomyopathy via the Kif15/TGF-β1 axis.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: